ArticleJournal of virology2005
Virus particle core defects caused by mutations in the human immunodeficiency virus capsid N-terminal domain.
Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 48 citations in OpenAlex.
- HIV-1 capsid variability: viral exploitation and evasion of capsid-binding molecules.Retrovirology · 2021Review
- Article
- CCR5 Inhibitors and HIV-1 Infection.Journal of AIDS and HIV treatment · 2019Article
- Inhibition of HIV-1 Maturation via Small-Molecule Targeting of the Amino-Terminal Domain in the Viral Capsid Protein.Journal of virology · 2017Article
- Contributions of Charged Residues in Structurally Dynamic Capsid Surface Loops to Rous Sarcoma Virus Assembly.Journal of virology · 2016Article
- Analysis of HIV-1 Gag protein interactions via biotin ligase tagging.Journal of virology · 2015Article
- High-throughput profiling of point mutations across the HIV-1 genome.Retrovirology · 2014Article
- Article
- Review
- Article
- Second site reversion of a mutation near the amino terminus of the HIV-1 capsid protein.Virology · 2013Article
- The NTD-CTD intersubunit interface plays a critical role in assembly and stabilization of the HIV-1 capsid.Retrovirology · 2013Article
- Slower uncoating is associated with impaired replicative capability of simian-tropic HIV-1.PloS one · 2013Article
- The interdomain linker region of HIV-1 capsid protein is a critical determinant of proper core assembly and stability.Virology · 2011Article
- New approaches for antiviral targeting of HIV assembly.Journal of molecular biology · 2011Review
- Antiviral activity of α-helical stapled peptides designed from the HIV-1 capsid dimerization domain.Retrovirology · 2011Article
- Second-site compensatory mutations of HIV-1 capsid mutations.Journal of virology · 2011Article
- Small-molecule inhibition of human immunodeficiency virus type 1 infection by virus capsid destabilization.Journal of virology · 2011Article
- Virtual screening based identification of novel small-molecule inhibitors targeted to the HIV-1 capsid.Bioorganic & medicinal chemistry · 2011Article
- Analysis of the N-terminal region of the murine leukemia virus nucleocapsid protein.Virus research · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The N-terminal domains (NTDs) of the human immunodeficiency virus type 1 (HIV-1) capsid (CA) protein have been modeled to form hexamer rings in the mature cores of virions. In vitro, hexamer ring units organize into either tubes or spheres, in a pH-dependent fashion. To probe factors which might govern hexamer assembly preferences in vivo, we examined the effects of mutations at CA histidine residue 84 (H84), modeled at the outer edges of NTD hexamers, as well as a nearby histidine (H87) in the cyclophilin A (CypA) binding loop. Although mutations at H87 yielded infectious virions, mutations at H84 produced assembly-competent but poorly infectious virions. The H84 mutant viruses incorporated wild-type levels of CypA and viral RNAs and showed nearly normal signals in virus entry assays. However, mutant CA proteins assembled aberrant virus cores, and mutant core fractions retained abnormally high levels of CA but reduced reverse transcriptase activities. Our results suggest that HIV-1 CA residue 84 contributes to a structure which helps control either NTD hexamer assembly or the organization of hexamers into higher-order structures.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.